ReviewFrontiers in oncology2020
Mitochondrial Redox Hubs as Promising Targets for Anticancer Therapy.
Review in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 54 citations in OpenAlex.
- Translational Pharmaceutical Perspectives on Quinones as Antioxidant and Antidiabetic Agents in Diabetes and Its Complications.Pharmaceutics · 2026Review
- Research advances in the pathogenesis and photodynamic therapy of pathological scars.Lasers in medical science · 2026Review
- The Role of Mitochondrial ROS in Neoplastic Transformations, Progression and Therapeutic Targeting.Oncology research · 2026Review
- Recent Advances in the Application of Mitochondria-targeted Fluorescent Probes.Current medicinal chemistry · 2025Review
- The Dose Rate of Corpuscular Ionizing Radiation Strongly Influences the Severity of DNA Damage, Cell Cycle Progression and Cellular Senescence in Human Epidermoid Carcinoma Cells.Current issues in molecular biology · 2024Article
- Polyphenolic Nanomedicine Regulating Mitochondria REDOX for Innovative Cancer Treatment.Pharmaceutics · 2024Review
- Article
- FUNDC1 predicts Poor Prognosis and promotes Progression and Chemoresistance in Endometrial Carcinoma.Journal of Cancer · 2024Article
- Targeting redox regulation and autophagy systems in cancer stem cells.Clinical and experimental medicine · 2023Review
- The mitochondrial calcium uniporter (MCU) activates mitochondrial respiration and enhances mobility by regulating mitochondrial redox state.Redox biology · 2023Article
- Mitochondria Transfer from Mesenchymal Stem Cells Confers Chemoresistance to Glioblastoma Stem Cells through Metabolic Rewiring.Cancer research communications · 2023Article
- Icaritin-loaded PLGA nanoparticles activate immunogenic cell death and facilitate tumor recruitment in mice with gastric cancer.Drug delivery · 2022Article
- Mitochondria Specific Antioxidant, MitoTEMPO, Modulates Cd Uptake and Oxidative Response of Soybean Seedlings.Antioxidants (Basel, Switzerland) · 2022Article
- Lentivirus-induced knockdown of IARS2 expression inhibits the proliferation and promotes the apoptosis of human osteosarcoma cells.Oncology letters · 2022Article
- Anticancer Aminoferrocene Derivatives Inducing Production of Mitochondrial Reactive Oxygen Species.Chemistry (Weinheim an der Bergstrasse, Germany) · 2022Article
- Article
- Article
- Effects of osteoblast-derived extracellular vesicles on aggressiveness, redox status and mitochondrial bioenergetics of MNNG/HOS osteosarcoma cells.Frontiers in oncology · 2022Article
- Reactive Oxygen Species Bridge the Gap between Chronic Inflammation and Tumor Development.Oxidative medicine and cellular longevity · 2022Review
- Role of Mitochondria in Radiation Responses: Epigenetic, Metabolic, and Signaling Impacts.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria play multifaceted roles in malignant tumor progression. Beyond their bioenergetic role, mitochondria are essential for providing malignant cells a higher plasticity to face the harsh environmental conditions. Cell-autonomous metabolic deregulation of cancer cells, or metabolic adaptation to microenvironmental cues (lack of nutrients, stromal supply, hypoxia, etc.), represent the triggering event of mitochondria overexploitation to orchestrate nutrient sensing and upload, signaling, and redox circuits. As readout of their higher function, mitochondria produce high amounts of reactive oxygen species (ROS) that are functional for multiple signaling networks underlying tumor proliferation, survival, and metastatic process. To compensate for the higher rate of mitochondrial ROS production, cancer cells have evolved adaptive mechanisms to increase their antioxidant systems and to address ROS activating pathways useful for the tumor cell adaptation to environmental changes. As these properties are critical for cancer progression, mitochondrial ROS have recently become an attractive target for anti-cancer therapies. We discuss how understanding of mitochondrial function in the tumor-specific generation of ROS will impact on the development of novel redox-based targeted therapeutic strategies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.